Vol. 274, Issue 4, R912-R920, April 1998
IGF-I alters lymphocyte survival and regeneration in thymus
and spleen after dexamethasone treatment
Pamela S.
Hinton,
Catherine A.
Peterson,
Elizabeth M.
Dahly, and
Denise M.
Ney
Department of Nutritional Sciences, University of Wisconsin-Madison,
Madison, Wisconsin 53706
Insulin-like growth factor I (IGF-I) is a
growth factor for the immune system, increasing lymphocyte number and
function via greater lymphocyte generation and/or survival. We
investigated the effects of IGF-I on lymphocyte survival and
regeneration in the thymus and spleen after dexamethasone (Dex)
treatment in rats maintained with parenteral nutrition and given
recombinant human IGF-I (800 µg/day) for 12 h, 48 h, and 5 days.
IGF-I did not prevent Dex-induced apoptosis of thymocytes but reduced
cell death in the spleen at 12 and 48 h. IGF-I exerted a modest
protective effect (10-15% reduction in cell loss) on all splenic
T and B cell subsets examined by flow cytometry. IGF-I enhanced
recovery of CD4+8+ immature T cells in the thymus and decreased the
proportion of CD8+ (cytotoxic/suppressor) T cells in the spleen. In
rats not treated with Dex, IGF-I significantly increased total
lymphocyte number and the number of CD4+8+ T cells in thymus and
spleen. Our results suggest that IGF-I may alter homeostasis in the
immune system by modulating lymphocyte generation and survival.
apoptosis; lymphopoiesis; insulin-like growth factor I; growth
factor; dexamethasone
